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. 2003 Jun 13;4(7):710–716. doi: 10.1038/sj.embor.embor882

Figure 2.

Figure 2

Characterization of the Endo180 deletion. (A) The left panel shows the results of RT–PCR (PCR after reverse transcription) reactions from +/+ and ΔEx2–6/ΔEx2–6 mouse embryonic fibroblasts (MEFs) using primers located in Endo180 exons 1 and 10. The products were resolved by agarose-gel electrophoresis. As a control, glyceraldehyde-3-phosphate dehydrogenase (Gapdh) PCR reactions were performed in parallel. Sequencing of the Endo180 RT–PCR product from ΔEx2–6/ΔEx2–6 cells identifies messenger RNA in which exon 1 is spliced onto the start of exon 7, and exons 2–6 are absent (right panel). (B) Membrane preparations from MEFs were resolved by SDS-polyacrylamide gel electrophoresis using 10% gels and were western blotted either with anti-Endo180 antibody followed by horseradish peroxidase (HRP)-conjugated anti-rabbit Ig, or with the anti-CD44 monoclonal antibody KM201 followed by HRP-conjugated anti-rat Ig (left panel). The right panel shows the structure of the wild-type Endo180 protein and the Endo180 protein from ΔEx2–6/ΔEx2–6 cells, which is missing the cysteine-rich (CR) domain, fibronectin type II (FNII) domain, C-type lectin domain 1 (CTLD1) and the first part of the CTLD1–CTLD2 linker region. The amino-terminal signal sequence is not shown. Cyto, cytoplasmic domain; TM, transmembrane domain.